Rong Liang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Rong Liang has a total of 23 co-authors. Here are the top co-authors by number of shared publications:
- Alex Rollo
Department of Experimental Diagnostic Imaging, The University of Texas MD Anderson Cancer Center, Houston, Tx 77030, USA
4 shared publications Archito T. Tamayo
4 shared publications- Jianfei Qian
Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH
4 shared publications - Jing Yang
Key Laboratory of Magnetic Molecules and Magnetic Information Materials of Ministry of Education & School of Chemistry and Materials Science of Shanxi Normal University, Taiyuan, 030032 China
4 shared publications John Lee
4 shared publications- Kate J. Newberry
The University of Texas MD Anderson Cancer Center, Houston, TX
4 shared publications
Latest Publications
- Open Access
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
Eight MCL Cell lines were cultured for 48 hours in the presence of different concentrations of CFZ. Cell growth was assessed by 3H-thymidine incorporation assay. The IC50 were determined by constructing a dose-response curve. Averages from 3 independent experiments are shown.
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
Eight MCL Cell lines were cultured for 48 hours in the presence of different concentrations of CFZ. Cell growth was assessed by 3H-thymidine incorporation assay. The IC50 were determined by constructing a dose-response curve. Averages from 3 independent experiments are shown.
- Open Access
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
Eight MCL Cell lines were cultured for 48 hours in the presence of different concentrations of CFZ. Cell growth was assessed by 3H-thymidine incorporation assay. The IC50 were determined by constructing a dose-response curve. Averages from 3 independent experiments are shown.
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
Eight MCL Cell lines were cultured for 48 hours in the presence of different concentrations of CFZ. Cell growth was assessed by 3H-thymidine incorporation assay. The IC50 were determined by constructing a dose-response curve. Averages from 3 independent experiments are shown.
- Open Access
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
PDF - 1267KB, The established MCL cell lines, JVM-2, JVM-13, MAVER, NCEB-1, and Z-138 were treated with 20 nM CFZ for 0, 6, 12, or 24 hours and apoptosis was detected by Annexin V-binding assays. Representative histograms (left panel) and percentages of apoptotic cells (right panel) are shown.
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
PDF - 1267KB, The established MCL cell lines, JVM-2, JVM-13, MAVER, NCEB-1, and Z-138 were treated with 20 nM CFZ for 0, 6, 12, or 24 hours and apoptosis was detected by Annexin V-binding assays. Representative histograms (left panel) and percentages of apoptotic cells (right panel) are shown.
- Open Access
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
PDF - 1267KB, The established MCL cell lines, JVM-2, JVM-13, MAVER, NCEB-1, and Z-138 were treated with 20 nM CFZ for 0, 6, 12, or 24 hours and apoptosis was detected by Annexin V-binding assays. Representative histograms (left panel) and percentages of apoptotic cells (right panel) are shown.
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 1 from In Vitro and In Vivo Therapeutic Efficacy of Carfilzomib in Mantle Cell Lymphoma: Targeting the Immunoproteasome
PDF - 1267KB, The established MCL cell lines, JVM-2, JVM-13, MAVER, NCEB-1, and Z-138 were treated with 20 nM CFZ for 0, 6, 12, or 24 hours and apoptosis was detected by Annexin V-binding assays. Representative histograms (left panel) and percentages of apoptotic cells (right panel) are shown.
- RetractedOpen Access
- 19 July 2021
- Published by Wiley in Journal of Oncology
- Vol. 2021, 1-10
All-Trans Retinoic Acid Enhances Chemosensitivity to 5-FU by Targeting miR-378c/E2F7 Axis in Colorectal Cancer
Colorectal carcinoma (CRC), a life-threatening malignancy, has been found to present resistance to 5-fluorouracil (5-FU) and cause a poor prognosis for patients. Previous studies have proved that all-trans retinoic acid (ATRA) could inhibit the development of CRC cells. In addition, miR-378c was discovered to exert a vital role in various cancers. In this study, we utilized MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), transwell assay, and flow cytometry to confirm that ATRA was able to enhance the inhibitory effects of 5-FU on HCT116 cells effectively by promoting cell apoptosis. Then, ENCORI database (http://starbase.sysu.edu.cn/) was employed to predict that miR-378c was downregulated dramatically in CRC and E2F7 was the direct target of miR-378c. QRT-PCR (quantitative real-time polymerase chain reaction) was conducted to verify that the expression level of miR-378c was decreased while E2F7 expression was upregulated in CRC tissues compared with para-carcinoma tissues. Additionally, treatment of 5-FU combined with ATRA could increase miR-378c expression, whereas it decreased the expression of E2F7. Dual-Luciferase Reporter assay results revealed that miR-378c could regulate the load of E2F7 by binding to its 3′UTR directly. Furthermore, miR-378c inhibitor or vector with E2F7 partially counteracted the effects of 5-FU combined with ATRA on viability, migration, invasion, and apoptosis of HCT116 cells. In conclusion, our study aims to confirm that ATRA enhances chemosensitivity to 5-FU of patients with CRC and expound the potential molecular mechanisms.
- 19 July 2021
- Published by Wiley in Journal of Oncology
- Vol. 2021, 1-10
RetractedOpen AccessAll-Trans Retinoic Acid Enhances Chemosensitivity to 5-FU by Targeting miR-378c/E2F7 Axis in Colorectal Cancer
Colorectal carcinoma (CRC), a life-threatening malignancy, has been found to present resistance to 5-fluorouracil (5-FU) and cause a poor prognosis for patients. Previous studies have proved that all-trans retinoic acid (ATRA) could inhibit the development of CRC cells. In addition, miR-378c was discovered to exert a vital role in various cancers. In this study, we utilized MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), transwell assay, and flow cytometry to confirm that ATRA was able to enhance the inhibitory effects of 5-FU on HCT116 cells effectively by promoting cell apoptosis. Then, ENCORI database (http://starbase.sysu.edu.cn/) was employed to predict that miR-378c was downregulated dramatically in CRC and E2F7 was the direct target of miR-378c. QRT-PCR (quantitative real-time polymerase chain reaction) was conducted to verify that the expression level of miR-378c was decreased while E2F7 expression was upregulated in CRC tissues compared with para-carcinoma tissues. Additionally, treatment of 5-FU combined with ATRA could increase miR-378c expression, whereas it decreased the expression of E2F7. Dual-Luciferase Reporter assay results revealed that miR-378c could regulate the load of E2F7 by binding to its 3′UTR directly. Furthermore, miR-378c inhibitor or vector with E2F7 partially counteracted the effects of 5-FU combined with ATRA on viability, migration, invasion, and apoptosis of HCT116 cells. In conclusion, our study aims to confirm that ATRA enhances chemosensitivity to 5-FU of patients with CRC and expound the potential molecular mechanisms.